Helicobacter pylori gastriti ve nonspesifik gastritlerde erken intestinal metaplazideki hücresel değişikliklerin CDX2 ile gösterilmesi ve bulguların histokimyasal yöntemlerle karşılaştırılması
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Tarih
2007
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info:eu-repo/semantics/openAccess
Özet
İntestinal metaplazi inflamasyon, atrofi, metaplazi, displazi ve kanser döngüsünde bir basamak olarak yerini almıştır. Metaplazi vücudun bir çok bölgesinde çeşitli nedenlerle oluşan koruyucu bir mekanizmadır. Fakat beklenmeyen bir yerde beklenmeyen bir değişimin olması farklı sonuçlara neden olmakta ve bu yeni oluşan durum her yönden daha az sağlam olmakta ve değişimlere daha açık olmaktadır. İntestinal metaplazi mekanizmasını, tetikleyen nedenler her zaman araştırma konusu olmuştur. Toplumda %50 gibi yüksek oranda görülen H. Pylori gastritinin intestinal metaplazinin gelişiminde rolü olup olmadığı ve hangi mekanizmalarla bunu yaptığı çoğu zaman merak edilmiştir. Bu amaçla Trakya Üniversitesi Tıp Fakültesi Patoloji Anabilim Dalı'ında 2000-2006 yılları arasındaki hem antrum hem de korpus bölgesinden alınan mide endoskopik biyopsilerine sahip gastrik kanser, peptik ülseri olmayan, H. Pylori için hiçbir tedavi almayan, dispeptik yakınmaları olan 85 hasta seçildi. Bu vakalar histopatolojik parametreler açısından, histokimyasal belirleyiciler (Alcian Blue Ph2,5 Periodic Acid Schiff, Alcian Blue Ph0,5 Periodic Acid Schiff), immünohistokimyasal belirleyiciler (CDX2, MUC2, MUC5AC) uygulanarak retrospektif olarak yeniden değerlendirildi. Sydney Update sisteme göre tekrar değerlendirilen vakaların tanısında değişiklik olmadı. Yaş ortalaması 47,4±17,8, 44(%51,8)'i erkek, 41(%48,2 )'si kadındı. Antrum biyopsilerinin %41,2'de korpus biyopsilerinin ise %49,4' H. Pylori varlığı tespit edildi. Antrumda 23 (%27,1) vakada İM, korpusta 13(%15,3) vakada İM tespit edildi. Tesbit edilen İM'nin tamamı komplet tip İM idi. MUC2 ile hem antrum hem de korpusda izlenen İM'nin tamamı pozitif olarak reaksiyon verdi (p=0.000). MUC2'nin intestinal epitele duyarlık ve seçiciliği %100 olarak bulundu. Bu nedenle MUC2'nin intestinal epitelin tanısında kullanılabilecek önemli bir belirteç olduğu saptandı. CDX2'nin İM'de antrumda %87, korpusta %92.3 oranında nükleer olarak eksprese edildiği gösterildi (p=0.000). MUC5AC intestinal epitel oluştuğu zaman intestinal epitelden salgılanmamaktadır. İM'de korpusta %100, antrumda ise %78.3 salgılanmadığı tesbit edildi (p=0.000). İnflamasyon, aktivite ve H. Pylori varlığında CDX2'nin sitoplazmik pozitifliği tespit edildi. Helicobacter Pylori varlığında CDX2'nin sitoplazmik ekspresyonu antrumda (%74.3), korpusta (%76.2) olarak tespit edildi ki H. Pylori'nin yaptığı inflamasyon CDX2'nin sitoplazmik salınımını uyarmakta olduğu saptanmıştır (p=0.000). Sitoplazmada oluşan bu genin ürünleri intestinal epitel oluştuğu zaman nükleusa kaymaktadır. İntestinal metaplazi mide kanserine giden süreçte bir basamaktır. Normalde intestinal kanal boyunca intestinal epitelin oluşumu, gelişimi ve düzenlenmesinde CDX2 bir orkestra şefi gibi rol almaktadır. İnflamasyonda ve H. Pylori varlığında CDX2'nin sitoplazmada var olması intestinal metaplazinin oluşmaya başlamasının bir bulgusudur. Bu bulgu intestinal epitelin genetik sürecini açıklamakta önemli adımdır. Bir genin ve ürünlerinin normalde olduğu yer dışında herhangi bir yerde bulunması o genin normal yerinde iken olduğu gibi indükleyen ve inhibe eden faktörleri beraberinde götürmemektedir. Bu da kanser sürecini başlatan bir mekanizma olabilir. CDX2 bu anlamda midenin intestinal tip adenokarsinomlarının tetikçisi olabilir. Bu açıdan bakıldığında bütün bu basamakların başlangıcı olan H. Pylori gastriti kanserin öncüsüdür denilebilir. Anahtar kelimeler: CDX2, intestinal metaplazi, Helicobacter Pylori, MUC2, MUC5AC.
Intestinal metaplasia took its place in the cycle of inflammation, atrophy, metaplasia and carcinoma. Metaplasia occurs in most parts of the body for many reasons. In fact metaplasia plays its role as a defensive mechanism of organs. However it leads to divergent results as it is an unexpected differentiation of unexpected localizations. This newly formed situation is less strong and less resistant to the external stimulants. Reasons that trigger mechanism of intestinal metaplasia has been sought for years. Whether H. Pylori gastritis which has an incidence of 50% in normal population plays a role and the way of its mechanism have been a popular topic of researches. Antral and corporal gastric endoscopic biopsies of 85 patients in period of 2000 to 2006, with dyspeptic symptoms and without any carcinoma and gastric ulcer and who did not receive any treatment for H. Pylori were taken into study in Pathology Department of Medical Faculty of Trakya University. Those cases were reviewed retrospectively concerning their histopathologic parameters by applying histochemical (Alcian Blue Ph2,5 Periodic Acid Schiff, Alcian Blue Ph0,5 Periodic Acid Schiff ) and immunohistochemical (CDX2, MUC2, MUC5AC ) markers. There was no change in the diagnosis of the cases which were reevaluated according to the Sydney update system. Mean age of the patients of whom 44 (51.8%) were men and 41 (48.2%) were women, was 47.4 ± 17.8. Intestinal metaplasia has been found in antrum of 23 (27,1%) cases and corpus of 13 (15,3%) cases. Intestinal metaplasia that have been diagnosed were all complete metaplasia. Intestinal epithelia of both antral and corporal biopsies were positive for MUC2 in all cases (p=0,000). MUC2 was demonstrated as an important marker for differential diagnosis of intestinal epithelia as its specifity and sensitivity for intestinal epithelium was 100%. CDX2 expression was shown to be 87% and 92.3 % in intestinal metaplastic epithelia of antrum and corpus respectively (p=0,000). MUC5AC is not secreted when the intestinal epithelium is formed. It is found that MUC5AC is not secreted in corpus (100%) and in antrum (78.3%) in the presence of intestinal epithelium (p= 0.000). Cytoplasmic reaction for CDX2 was of attention in the presence of inflammation, activity and positivity for H. Pylori which was 74.3% and 76.2% in antrum and corpus respectively. As a result, it was found out that, inflammation due to H. Pylori stimulates the cytoplasmic secretion of CDX2 (p=0,000). Cytoplasmic products of this gene migrate to nucleus when intestinal epithelium is formed. Intestinal metaplasia is a step on the way to gastric carcinoma. In normal conditions CDX2 plays a chief role in the formation, proliferation and organization of intestinal epithelium in the intestinal tract. Presence of CDX2 in the cytoplasm in presence of inflammation and H. Pylori is a sign of beginning of formation of intestinal metaplasia. This finding is an important step in defining the genetic mechanism of intestinal epithelium. This may be the mechanism that triggers the formation of carcinoma and CDX2 may be the factor that triggers the intestinal type of adenocarcinomas of the stomach. From this point of view, H. Pylori gastritis can be defined as the initiator for carcinoma. Key words: CDX2, Intestinal Metaplasia, Helicobacter pylori, MUC2, MUC5AC
Intestinal metaplasia took its place in the cycle of inflammation, atrophy, metaplasia and carcinoma. Metaplasia occurs in most parts of the body for many reasons. In fact metaplasia plays its role as a defensive mechanism of organs. However it leads to divergent results as it is an unexpected differentiation of unexpected localizations. This newly formed situation is less strong and less resistant to the external stimulants. Reasons that trigger mechanism of intestinal metaplasia has been sought for years. Whether H. Pylori gastritis which has an incidence of 50% in normal population plays a role and the way of its mechanism have been a popular topic of researches. Antral and corporal gastric endoscopic biopsies of 85 patients in period of 2000 to 2006, with dyspeptic symptoms and without any carcinoma and gastric ulcer and who did not receive any treatment for H. Pylori were taken into study in Pathology Department of Medical Faculty of Trakya University. Those cases were reviewed retrospectively concerning their histopathologic parameters by applying histochemical (Alcian Blue Ph2,5 Periodic Acid Schiff, Alcian Blue Ph0,5 Periodic Acid Schiff ) and immunohistochemical (CDX2, MUC2, MUC5AC ) markers. There was no change in the diagnosis of the cases which were reevaluated according to the Sydney update system. Mean age of the patients of whom 44 (51.8%) were men and 41 (48.2%) were women, was 47.4 ± 17.8. Intestinal metaplasia has been found in antrum of 23 (27,1%) cases and corpus of 13 (15,3%) cases. Intestinal metaplasia that have been diagnosed were all complete metaplasia. Intestinal epithelia of both antral and corporal biopsies were positive for MUC2 in all cases (p=0,000). MUC2 was demonstrated as an important marker for differential diagnosis of intestinal epithelia as its specifity and sensitivity for intestinal epithelium was 100%. CDX2 expression was shown to be 87% and 92.3 % in intestinal metaplastic epithelia of antrum and corpus respectively (p=0,000). MUC5AC is not secreted when the intestinal epithelium is formed. It is found that MUC5AC is not secreted in corpus (100%) and in antrum (78.3%) in the presence of intestinal epithelium (p= 0.000). Cytoplasmic reaction for CDX2 was of attention in the presence of inflammation, activity and positivity for H. Pylori which was 74.3% and 76.2% in antrum and corpus respectively. As a result, it was found out that, inflammation due to H. Pylori stimulates the cytoplasmic secretion of CDX2 (p=0,000). Cytoplasmic products of this gene migrate to nucleus when intestinal epithelium is formed. Intestinal metaplasia is a step on the way to gastric carcinoma. In normal conditions CDX2 plays a chief role in the formation, proliferation and organization of intestinal epithelium in the intestinal tract. Presence of CDX2 in the cytoplasm in presence of inflammation and H. Pylori is a sign of beginning of formation of intestinal metaplasia. This finding is an important step in defining the genetic mechanism of intestinal epithelium. This may be the mechanism that triggers the formation of carcinoma and CDX2 may be the factor that triggers the intestinal type of adenocarcinomas of the stomach. From this point of view, H. Pylori gastritis can be defined as the initiator for carcinoma. Key words: CDX2, Intestinal Metaplasia, Helicobacter pylori, MUC2, MUC5AC
Açıklama
Anahtar Kelimeler
Patoloji, Pathology
